Morphologic and metabolic studies of normal and traumatized vitreous will be used to determine cellular and biochemical reactions following injury. Injections of autologous blood into the vitreous of rabbits and hyperoxygenation of newborn mice and/or kittens will be used as models of vitreous hemorrhage and attempts made to correlate histologic and metabolic changes with the usual clinical sequence of hemorrhage, formation of condensed vitreous strands,scarring, and contraction. Light and electron microscopy will be utilized to determine changes in the number and types of vitreous cells and the nature of hyalocyte and fibrocyte production. The chronological sequence of collagen production, its cellular origin, and changes in type following vitreous hemorrhage will also be investigated using radioautography and analysis of CNBr peptide patterns. On the assumption that hyaluronic acid depolymerization leading to liquefaction and collapse of the vitreous is the major stimulus to subsequent reactive events, it is proposed that this is initiated by exposure to superoxide free radicals released by phagocytizing leukocytes. These hypotheses will be tested by investigation the origin and role of free radicals in vitreous reactions and the therapeutic efficacy of endogenous and exogenous superoxide dismutase, a free radical scavenger, in the prevention of vitreous scarring determined. Levels of lysyl oxidase activity in normal and traumatized vitreous will be measured to determine if increased activity is correlated with scarring and contraction resulting from greater collagen cross-linkage. Beta-aminopropionitrile, an inhibitor of lysyl oxidase, will be administered to determine its potential therapeutic role in the inhibition of vitreous contraction following injury.